{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T07:23:44Z","timestamp":1771658624584,"version":"3.50.1"},"reference-count":40,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2022,6,23]],"date-time":"2022-06-23T00:00:00Z","timestamp":1655942400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Laboratory Analysis"],"published-print":{"date-parts":[[2022,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Epigenetic abnormalities in acute myeloid leukaemia provide us with a target for novel therapeutic strategies. The aim of the study was to verify the epigenetic regulatory mechanism of <jats:italic>E\u2010cadherin<\/jats:italic> gene silencing induced by long non\u2010coding RNA MALAT\u20101 in AML.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Expression of MALAT\u20101, <jats:italic>E\u2010cadherin<\/jats:italic>, <jats:italic>EZH2<\/jats:italic>, <jats:italic>SUZ12<\/jats:italic> and <jats:italic>EED<\/jats:italic> genes in AML patients was detected by RT\u2010qPCR. After MALAT\u20101 silencing in AML cell lines, levels of the <jats:italic>E\u2010cadherin<\/jats:italic>, <jats:italic>EZH2<\/jats:italic>, <jats:italic>SUZ12<\/jats:italic>, <jats:italic>EED<\/jats:italic>, <jats:italic>DNMT1<\/jats:italic>, <jats:italic>DNMT3A<\/jats:italic> and <jats:italic>DNMT3B<\/jats:italic> genes and encoded proteins were detected by RT\u2010qPCR and Western blotting. The level of CpG island methylation and trimethylation modification of histone H3K27 in the promoter region of <jats:italic>E\u2010cadherin<\/jats:italic> was detected by pyrosequencing and ChIP\u2010qPCR. RIP\u2010qPCR was used to detect the interaction between MALAT\u20101 and proteins.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>MALAT\u20101, <jats:italic>EZH2<\/jats:italic> and <jats:italic>EED<\/jats:italic> gene expression was markedly increased in AML patients with <jats:italic>E\u2010cadherin<\/jats:italic> down\u2010regulation. A positive correlation between <jats:italic>EZH2<\/jats:italic> or <jats:italic>SUZ12<\/jats:italic> and MALAT\u20101 expression was observed. After MALAT\u20101 silencing, the expression of <jats:italic>E\u2010cadherin<\/jats:italic> was up\u2010regulated, whereas the expression of <jats:italic>EZH2<\/jats:italic>, <jats:italic>SUZ12<\/jats:italic>, <jats:italic>DNMT1<\/jats:italic>, <jats:italic>DNMT3A<\/jats:italic> and <jats:italic>DNMT3B<\/jats:italic> was down\u2010regulated. Results of Western blotting were consistent with those of RT\u2010qPCR. Methylation levels of <jats:italic>E\u2010cadherin<\/jats:italic> in AML patients were higher than that in normal controls, which appeared to increase with age. Methylation of the CpG island and H3K27 trimethylation of <jats:italic>E\u2010cadherin<\/jats:italic> were decreased after MALAT\u20101 silencing. RIP\u2010qPCR suggested that MALAT\u20101 might be enriched by EZH2 and SUZ12.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our findings verified that MALAT\u20101 might lead to the transcriptional silencing of E\u2010cadherin gene through the trimethylation of H3K27 mediated by recruiting EZH2 and SUZ12.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcla.24556","type":"journal-article","created":{"date-parts":[[2022,6,24]],"date-time":"2022-06-24T06:39:18Z","timestamp":1656052758000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Epigenetic silencing of <i>E\u2010cadherin<\/i> gene induced by <scp>lncRNA MALAT<\/scp>\u20101 in acute myeloid leukaemia"],"prefix":"10.1002","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4179-5001","authenticated-orcid":false,"given":"Jinlong","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Hematology First 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